神经科学通报(英文版)
神經科學通報(英文版)
신경과학통보(영문판)
NEUROSCIENCE BULLETIN
2008年
2期
117-123
,共7页
溶酶体%组织蛋白酶%坏死%凋亡%自噬%脑缺血
溶酶體%組織蛋白酶%壞死%凋亡%自噬%腦缺血
용매체%조직단백매%배사%조망%자서%뇌결혈
lysosomes%cathepsin%necrosis%apoptosis%autophagy%cerebral ischemia
细胞死亡有凋亡(Ⅰ型)、自噬性细胞死亡(Ⅱ型)和坏死(Ⅲ型)三种方式.缺血性神经元的死亡影响着中风的发展进程.溶酶体是一种重要的细胞器,通过在酸性环境中降解不需要的胞外和胞内物质来维持细胞代谢的稳态.溶酶体酶包括组织蛋白酶和脂质水解酶,当溶酶体膜破裂时它们会被释放到细胞浆,会对细胞内环境产生危害,最终导致细胞结构的破坏.由于溶酶体含有催化蛋白、碳水化合物和脂质的酶;因此它们参与细胞的死亡看起来是情理之中的事情.本综述讨论了缺血性神经元死亡的最新进展,指出在缺血性脑损伤中溶酶体酶参与三种细胞死亡方式的可能的分子机制,同时指出了选择性的组织蛋白酶抑制剂可能是治疗中风和促进康复新的治疗靶点.
細胞死亡有凋亡(Ⅰ型)、自噬性細胞死亡(Ⅱ型)和壞死(Ⅲ型)三種方式.缺血性神經元的死亡影響著中風的髮展進程.溶酶體是一種重要的細胞器,通過在痠性環境中降解不需要的胞外和胞內物質來維持細胞代謝的穩態.溶酶體酶包括組織蛋白酶和脂質水解酶,噹溶酶體膜破裂時它們會被釋放到細胞漿,會對細胞內環境產生危害,最終導緻細胞結構的破壞.由于溶酶體含有催化蛋白、碳水化閤物和脂質的酶;因此它們參與細胞的死亡看起來是情理之中的事情.本綜述討論瞭缺血性神經元死亡的最新進展,指齣在缺血性腦損傷中溶酶體酶參與三種細胞死亡方式的可能的分子機製,同時指齣瞭選擇性的組織蛋白酶抑製劑可能是治療中風和促進康複新的治療靶點.
세포사망유조망(Ⅰ형)、자서성세포사망(Ⅱ형)화배사(Ⅲ형)삼충방식.결혈성신경원적사망영향착중풍적발전진정.용매체시일충중요적세포기,통과재산성배경중강해불수요적포외화포내물질래유지세포대사적은태.용매체매포괄조직단백매화지질수해매,당용매체막파렬시타문회피석방도세포장,회대세포내배경산생위해,최종도치세포결구적파배.유우용매체함유최화단백、탄수화합물화지질적매;인차타문삼여세포적사망간기래시정리지중적사정.본종술토론료결혈성신경원사망적최신진전,지출재결혈성뇌손상중용매체매삼여삼충세포사망방식적가능적분자궤제,동시지출료선택성적조직단백매억제제가능시치료중풍화촉진강복신적치료파점.
There are three different types of cell death, including apoptosis (Type Ⅰ), autophagic cell death (Type Ⅱ), and necrosis (Type Ⅲ). Ischemic neuronal death influences stroke development and progression. Lysosomes are important organelles having an acidic milieu to maintain cellular metabolism by degrading unneeded extra- and intracellular substances. Lysosomal enzymes, including cathepsins and some lipid hydrolases, when secreted following rupture of the lysosomal membrane, can be very harmful to their environment, which results in pathological destruction of cellular structures. Since lysosomes contain catalytic enzymes for degrading proteins, carbohydrates and lipids, it seems natural that they should participate in cellular death and dismantling. In this review, we discuss the recent developments in ischemic neuronal death, and present the possible molecular mechanisms that the lysosomal enzymes participate in the three different types of cell death in ischemic brain damage. Moreover, the research related to the selective cathepsin inhibitors may provide a novel therapeutic target for treating stroke and promoting recovery.